Difference between revisions of "Gulonolactone oxidase"
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| − | '''Gulonolactone oxidase''' is an enzyme that catalyzes the reactions needed to produce [[ascorbic acid]] (vitamin | + | '''Gulonolactone oxidase''' is an enzyme that catalyzes the reactions needed to produce [[ascorbic acid]] (vitamin C). <ref>''Molecular basis for the deficiency in humans of gulonolactone oxidase, a key enzyme for ascorbic acid biosynthesis'', American Journal of Clinical Nutrition, Vol 54, 1203S-1208S [http://www.ajcn.org/cgi/content/abstract/54/6/1203S] </ref> |
This gene is present in most animals however it has been inactivated due to mutation in some. Animals that can no longer synthesize vitamin c include: [[simians]], [[guinea pig]]s, and several species of [[fruit bat]]s. Since these organisms consume a large portion of their diet in fruit the inactivation of the gene was not a significant detriment. Humans that fail to eat sources of vitamin c can develop [[scurvy]]. | This gene is present in most animals however it has been inactivated due to mutation in some. Animals that can no longer synthesize vitamin c include: [[simians]], [[guinea pig]]s, and several species of [[fruit bat]]s. Since these organisms consume a large portion of their diet in fruit the inactivation of the gene was not a significant detriment. Humans that fail to eat sources of vitamin c can develop [[scurvy]]. | ||
Revision as of 15:01, May 24, 2007
Gulonolactone oxidase is an enzyme that catalyzes the reactions needed to produce ascorbic acid (vitamin C). [1] This gene is present in most animals however it has been inactivated due to mutation in some. Animals that can no longer synthesize vitamin c include: simians, guinea pigs, and several species of fruit bats. Since these organisms consume a large portion of their diet in fruit the inactivation of the gene was not a significant detriment. Humans that fail to eat sources of vitamin c can develop scurvy.
The mutation that causes the inactivation of the L-gulonolactone oxidase gene is different depending on the group the organism is in. All extant Guinea pigs share the same inactivation mutation, while all extant simians share a different one. The likelihood of two different species sharing the same inactivation mutation is statistically impossible and is actually shared due to common inheritance. The most recent common ancestor of all extant guinea pigs developed the mutation in the gene, while a different mutation developed in the most recent common ancestor in simians.
There are multiple examples of these kinds of inactivated genes across all extant species, the term pseudogenes is used to label all of these.
See also
References
- ↑ Molecular basis for the deficiency in humans of gulonolactone oxidase, a key enzyme for ascorbic acid biosynthesis, American Journal of Clinical Nutrition, Vol 54, 1203S-1208S [1]
External links
- http://www.ihop-net.org/UniPub/iHOP/gismo/88910.html GLUOP from IHOP
